Neurotrauma Flashcards
Breathing patterns associated with damage to
a) cerebrum
b) pons
c) medulla
a) Cheyne stokes (alternating hyperpneoa and apnoea)
b) apneustic (prolonged pause at end inspiration)
c) ataxic (irregular in rate and volume)
How is the size of an intracerebral haematoma calculated
(a x b x c) / 2
a=maximum haematoma diameter
b=haematoma diameter at 90 degrees to a
c=number of CT slides with haematoma visible x slice thickness
How is CPP calculated
MAP - ICP
How is MAP calculated
2/3 diastole + 1/3 systole
In which patients should ICP be monitored
GCS 3-8 with abnormal CT
How is RICP managed?
ventilate and oxygenate keep CO2 at the low end of normal (4) nurse at 30 degree angle mannitol 100ml 20% paralyse (to reduce cerebral O2 requirements) normoglycaemia phenytoin for seizures
What are the advantages and disadvantages of paralysing a patient in RICP management?
reduces cerebral O2 requirements
allows TTM
can’t assess any progress
Define mild, moderate and severe TBI according to GCS
mild: 14-15
mod: 9-13
severe: <9
What is a primary head injury
Injury occurring at the time of the impact. Can be vascular, neuronal, axonal
What is a secondary head injury
processes occurring later down the line that has been triggered by the primary head injury
State some examples of processes that can occur as part of a secondary head injury
ischaemia hypoxia neuroinflammation (cytokines and chemokines) RICP infection seizures mitochondrial dysfunction
What is a tertiary/late secondary head injury
injury occurring years after the primary injury. Thought to be due to proteinopathies. Patients can present with MND, Parkinsons, alzheimers, fronto-temporal dementia
What are some faults with GCS
skewed important to motor
can’t assess if facial/ocular injury
can’t assess if intubated
designed for purely head injured patients
Talk through the eye component of GCS
4: spontaneous eye opening
3: open to verbal command
2: open to pain
1: no response
Talk through the verbal component of GCS
5: orientated
4: confused
3: inappropriate words
2: incomprehensible sounds
1: no response
Talk through the motor component of GCS
6: spontaneous movements
5: localise pain
4: withdraw from pain
3: flexion (decorticate)
2: extension (decerebrate)
1: no response
What should you examine in a possible head injury patient
breathing pattern pupils ocular movements (cranial nerves) c-spine auscultate the carotids limb movements and power
Indications for a CT after a head injury
GCS <13 GCS <15 after 2 hours >1 episode of vomiting open, depressed or basal skull fracture seizure focal deficit
Compare the appearance of a T1 and T2 weighted MRI
T1: black CSF. Grey matter is grey and white matter is white
T2: bright CSF. Grey matter is white and white matter is grey
What does acute and hyperacute blood look like on a CT
acute is hyperdense (bright)
hyperacute can appear as a darker patch within the bright acute bleed
What motion often causes DAI
rotational
acceleration/deceleration
What is the pathophysiology of DAI
sheering of G/W matter interface
wallerian degeneration distal to the sheering forces
What is the CT appearance of DAI
homogenous loss of G/W matter interface
scattered punctae
What is a cerebral contussion
microhaemorrhages and small vessel leaks
They are <1cm
where are contussions most likely to occur
inferior frontal
temporal poles
these are both sharp and ridgy areas
State some clinical features suggestive of a basal skull fracture
racoon eyes battles sign CSF rhinorrhoea and ottorhoea haemotympanum CN signs
Where is a basal skull fracture most likely to occur
longitudinal fracture of the petrous part of the temporal bone
what is a concussion
temporary alteration of consciousness
no structural damage
absence of a penetrating injury
compare the bleeding source associated with extradural vs subdural vs subarachnoid haematomas
extra: middle meningeal artery or DVS
subdural: cortical bridging veins
subarachnoid: berry anneurysm, AV malformation
what is the likely source of bleeding in a posterior fossa bleed
DVS
where does the middle meningeal artery originate and which foramen does it travel through
maxillary artery (branch of ECA) foramen spinosum
describe the clinical presentation of extradural, subdural and subarachnoid haemorrhages
extra: lucid interval
subdural: presents like an evolving stroke
subarachnoid: occipital thunderclap headache
Describe the CT of an extradural haematoma
lenticuloform
limited by suture lines
describe the CT of a subdural haematoma
crescent
not limited by suture lines
can enter sulci
loss of G/W matter interface
describe the CT of a subarachnoid haematoma
hyperdense basal cisterns and sulci
What 2 mechanisms lead to ischaemia in secondary brain injury
blood is an irritant so get vasospasm
RICP leads to reduced CPP
how does cerebral oedema occur in secondary brain injury
extracellular to intracellular because of NaK pump failure
intravascular to interstitial because of BBB breakdown
Describe the Monro-Kellie hypothesis
Pressure-volume relationship aiming to keep a dynamic equilibrium among non-compressible components in a rigid skull.
Components within the fixed rigid skull will compensate for an increased intracranial volume up until a point at which ICP begins to rise
What are the x and y axis on the monro-kellie graph
x: intracranial volume
y: ICP
Describe cushings reflex
Hypertension: brainstem compression stimulates sympathetics to try and overcome the ICP and maintain CPP
Bradycardia: in response to the hypertension the carotid sinus stimulates a vagal response
reduced RR: ischaemia of the respiratory centers in the brainstem
State the types of herniation syndrome
subfalcine
uncul
tonsillar
what is compressed in a subfalcine herniation and what does this result in clinically
the cingulate gyrus is compressed under the falx cerebri
ACA compressed leading to contralateral leg weakness
what is compressed in a uncal herniation and what does this result in clinically
uncus of the temporal lobe
CN3: ipsilateral dilated, down and out pupil
CN6: diplopia
reticular formation: reduced GCS
cerebellar peduncle: contralateral hemiparesis
Describe kernohans phenomenon
contra-lateral cerebellar peduncle compressed where the descending motor tracts are located giving ipsilateral (to the lesion) motor weakness
what is compressed in a tonsillar herniation and what does this result in clinically
cerebellar tonsils compressed through the foramen magnum
cardioresp centres in medulla compressed
How can ICP be measured
ICP bolt
intraventricular catheter
intraparenchymal pressure monitor
Define secondary brain injury
progressive series of complex, interconnected, biochemical events all ending in neuronal death
craniotomy vs craniectomy
craniotomy: bone is replaced
craniectomy: bone is left off and the skin flap closed
what are mayfield pins
hold the head in place whilst a craniectomy/otomy is performed
why do burr holes tend not to work in haematoma management
because the blood is thick and clotted
which type of haematoma might a burr hole work and why
chronic subdural when the blood has gone back to a liquid
what is secondary impact syndrome
seen in younger patients
following a concussion there is malignant oedema
anterograde vs retrograde amnesia
anterograde: can’t form new memories
retrograde: inability to recall past memories
when should a neurosurgeon become involved in head injury patients
GCS <8 or deteriorating Confusion >4 hours progressive focal neurological signs seizure without full recovery depresed skull fracture penetrating injury CSF leakage
